NF-κB activation in organs from STZ-treated rats

Nuclear factor kappa B (NF-κB) is a ubiquitously expressed transcription factor comprised of various subunits (p50 (NF-κB1), p52 (NF-κB2), p65 (RelA), RelB, and c-Rel). Activation of certain NF-κB subunits appears to foster an inflammatory state that may promote the development of disease. Thus characterizing the specific NF-κB subunits may provide insight into the pathogenesis of certain diseases. The purpose of this study was to determine if 1 month of a diabetic state, induced by streptozotocin (STZ) treatment, alters the constitutive level of NF-κB activation, its subunit composition, or the content of NF-κB-related proteins in rodent liver, kidney, spleen, and heart. Diabetes was induced in male Sprague-Dawley rats by a single tail vein injection of STZ (55 mg·kg-1 body weight). After 30 days, the heart, liver, spleen, and kidney were assessed for NF-κB activation and subunit composition with electrophoretic mobility shift assay (EMSA), and p50 and p65 subunit content was assessed with Western blotting. In diabetic animals, the constitutive level of NF-κB activation was reduced in liver, but was unchanged in kidney, spleen, and heart. EMSA supershifts showed the predominant subunit in the activated NF-κB complexes from both diabetic and control animals to be p50, although the p65 subunit was detected in NF-κB complexes from diabetic hearts. The content of p50 was unaltered in all diabetic tissues examined, whereas the content of p65 was increased only in hearts from diabetic animals. These findings support the idea that a diabetic state may induce specific changes in NF-κB subunit composition in certain tissues.